Replication-dependent Z-ring formation (RDZ) : interruption of DNA replication blocks cell division independently of nucleoid occlusion and the SOS response in E. coli

Chromosome replication and cell division of Escherichia coli are coordinated with growth such that wild-type cells divide once and only once after each replication cycle. Two components of this coordination are the SOS system and nucleoid occlusion. The SOS regulon expresses DNA repair genes after DNA damage and delays FtsZ-ring formation and cell division to enhance survival. Nucleoid occlusion prevents cell division over un-replicated nucleoids, a process partially dependent on the SlmA protein. Z-ring formation is shown here to be dependent on DNA replication by an additional mechanism, independent of the SOS regulon and of the SlmA protein and which acts by preventing FtsZ-ring formation when replication is perturbed. Replication dependent Z-ring formation (RDZ) was shown to be SOS-independent by the fact that FtsZ-rings were inhibited, after replication blockage, in a lexA1 mutant and in strains containing a null allele of sulA or the ftsZ/sulB103 mutation. SlmA protein-independence was shown by the fact that FtsZ-rings were also inhibited in lexA1 [Delta]slmA double mutants after replication blockage. This SOS- and SlmA-independent mechanism functions effectively in cells growing slowly with only one replicating chromosome and also in cells growing rapidly with multi-fork replication and after replication inhibition by different methods - chemical inhibitors and a temperature-sensitive polymerization mutation.